Antithrombotic Therapy After Percutaneous Coronary Intervention in Atrial Fibrillation: The Triple Trouble.

One of the most common conundrums in all cardiovascular medicine pertains to the care of patients with atrial fibrillation after percutaneous coronary intervention, because of both dual antiplatelet therapy and oral anticoagulant therapy would seem to be necessary to reduce risks of stent thrombosis and thromboembolism, respectively, but also with an inevitable trade-off of more bleeding. Patients who require triple therapy are at high risk of both ischaemia and bleeding; therefore, defining a personalised secondary prevention strategy aimed at achieving the best net clinical benefit is essential. The good news is that we have entered an era of increased perceived and tangible safety that applies to both non-vitamin K-antagonist oral anticoagulants and newer drug-eluting stents. Even if the consistency across the major trials and the significantly lower risk of bleeding with dual therapy make it hard to argue that triple therapy should be used routinely, the aggregate evidence suggests that the net clinical benefit of dual therapy should give cardiologists confidence to drop aspirin when they are using a contemporary percutaneous coronary intervention strategy with drug-eluting stents. Waiting for more randomised trials and meta-analyses, for the time being, in patients not in clinical trials, full-dose oral triple therapy with dual antiplatelet agents and full-dose anticoagulation should be avoided as a routine practice, and the choice of the proper, that is, safer, oral anticoagulant, namely a non-vitamin K-antagonist oral anticoagulant, may be regarded by now as an additional bleeding avoiding strategy in patients with atrial fibrillation undergoing percutaneous coronary intervention.

The relationship between obesity and hypertension: an updated comprehensive overview on vicious twins.

Obesity is a growing global health concern, with a rapid increase being observed in morbid obesity. Obesity is associated with an increased cardiovascular risk and earlier onset of cardiovascular morbidity. The growing obesity epidemic is a major source of unsustainable health costs and morbidity and mortality because of hypertension, type 2 diabetes mellitus, dyslipidemia, certain cancers and major cardiovascular diseases. Similar to obesity, hypertension is a key unfavorable health metric that has disastrous health implications: currently, hypertension is the leading contributor to global disease burden, and the direct and indirect costs of treating hypertension are exponentially higher. Poor lifestyle characteristics and health metrics often cluster together to create complex and difficult-to-treat phenotypes: excess body mass is such an example, facilitating a cascade of pathophysiological sequelae that create such as a direct obesity-hypertension link, which consequently increases cardiovascular risk. Although some significant issues regarding assessment/management of obesity remain to be addressed and the underlying mechanisms governing these disparate effects of obesity on cardiovascular disease are complex and not completely understood, a variety of factors could have a critical role. Consequently, a comprehensive and exhaustive investigation of this relationship should analyze the pathogenetic factors and pathophysiological mechanisms linking obesity to hypertension as they provide the basis for a rational therapeutic strategy in the aim to fully describe and understand the obesity-hypertension link and discuss strategies to address the potential negative consequences from the perspective of both primordial prevention and treatment for those already impacted by this condition.

Hypertensive response to exercise and exercise training in hypertension: odd couple no more.

The diagnostic and prognostic implication of exaggerated blood pressure response to exercise has been controversial, with opinions ranging from a benign process to a harbinger of potential cardiovascular morbidity. Nonetheless, lowering of blood pressure and prevention of hypertension is in first instance preferable by lifestyle changes, and many studies have shown the inverse association between physical activity level and the incidence of cardiovascular diseases suggesting low aerobic fitness as a strong predictor for future cardiovascular disease and all-cause mortality in both healthy and cardiovascular disease patients, including those with hypertension. Endothelial function, large artery stiffness and neurohormonal response are surely implicated both in the development of exaggerated blood pressure response to exercise and in the positive effect of physical exercise in the prevention and management of hypertension and cardiovascular disease in general. In their interesting and well documented review published in this issue Kim and Ha broadly described the possible pathophysiologic mechanisms of exaggerated blood pressure response to exercise and its clinical implications: in this regard, a very interesting issue could be represented by the role of exercise training. In fact, there is an the ample evidence in the literature that physical activity could positively affect endothelial function, arterial stiffness, neurohormonal response and finally blood pressure levels both in healthy men and in hypertensive patients and so should be considered a very important element in the prevention and management of cardiovascular disease.